Targeting Mitochondrial Calcium Handling and Reactive Oxygen Species in Heart Failure

Author:

Dietl Alexander,Maack Christoph

Publisher

Springer Science and Business Media LLC

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Emergency Medicine

Reference172 articles.

1. Münzel T, Camici G, Maack C, Bonetti N, Fuster V, Kovacic J. Impact of oxidative stress on the heart and vasculature. J. Am. Coll. Cardiol. 2017;in press.

2. Yusuf S, Dagenais G, Pogue J, Bosch J, Sleight P. Vitamin E supplementation and cardiovascular events in high-risk patients. The heart outcomes prevention evaluation study investigators. N Engl J Med. 2000;342:154–60.

3. •• Nickel AG, von Hardenberg A, Hohl M, Löffler JR, Kohlhaas M, Becker J, et al. Reversal of mitochondrial transhydrogenase causes oxidative stress in heart failure. Cell Metab. 2015;22:472–84. In this paper, we discovered a novel mechanism how pathological cardiac workload increases oxidative stress in mitochondria, and that this oxidative stress played a causal role in the development of heart failure. It also suggests that targeting mitochondria with SS-31 to reduce oxidative stress rescued mortality in mice with heart failure.

4. Kohlhaas M, Nickel AG, Maack C. Mitochondrial energetics and calcium coupling in the heart. J Physiol. 2017;595:3753–3763.

5. •• Fujikawa Y, Roma LP, Sobotta MC, Rose AJ, Diaz MB, Locatelli G, et al. Mouse redox histology using genetically encoded probes. Sci Signal. 2016;9:rs1. In this paper, a novel mouse model was developed with which oxidative stress can be analyzed in mitochondria of virtually any organ of interest, with high spatial resolution to discriminate different cell types within an organ. The technique uses histological analysis of a redox-based reporter protein that is highly sensitive and specific for hydrogen peroxide (H 2 O 2 ).

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